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Diurnal levels of serum triglyceride, cholesterol, free fatty acids, glucose, and cortisol were measured in four normal persons on a fixed solid 65% carbohydrate diet under steady state conditions in a metabolic unit. Triglyceride levels in all subjects showed similar patterns, which unexpectedly did not bear a simple relation to meal frequency or distribution. With three equivalent meals per day at 09.00, 12.00 and 17.00 hours, 'fasting' triglyceride levels increased by about 0.3 g/l from a minimum value between 03.00 and 05.00 hours in the morning till before breakfast. After breakfast there was a continued rise till about 15.00 hours and then a overall fall in spite of the meal at 17.00 hours. Isocaloric change to eight equivalent meals, consumed between 09.00 and 23.00 hours, resulted in a similar although slightly more even triglyceride pattern. On eight equivalent meals, spaced evenly over the entire 24 h period, a different pattern was found with lower triglyceride values at daytime than at night. Increase in meal frequency did not result in a lowering of mean diurnal triglyceride levels. The cholesterol pattern followed the triglyceride pattern most clearly in subjects with high triglyceride levels. Glucose showed the expected postprandial increments. Cortisol rhythm did not change on varying meal frequency.

253Table Posthyperglycemic glucose and insulin areas and insulin/glucose area ratios in obese subjects with asymptomatic reactive hypoglycemia and obese control subjects (Mean ± Se) * p < 0.05 Obese hypoglycemics Obese controls Posthyperglycemic glucose area (mg/dl'min) 9,537.5 ± 393.1 * 10,668.1 ± 400.1These data suggest that relative excess in posthyperglycemic insulin secretion in obese hypoglycemic subjects in comparison with obese controls-decreases the ability to maintain glucose homeostasis. This is also supported by the results of McCool, Luqman, Schmitt, Raymundo, Nolan, Stephan, Ah· mad and Danowski (1977) who found that in some instances of reactive hypoglycemia concomitant insulin values were higher than starting levels. However it seems that increased posthyperglycemic insulin area and increased insulin/glucose area ratio are more related to blood glucose nadir than relatively increased rnatched insulin values.Impared insulin-glucose balance in posthyperglycemic period of glucose tolerance test is a strong evidence that asymptomatic reactive hypoglycemia in obesity is not a physiological variation, but, probably, an early diabetic condition.Requests for reprints should be addressed to: M. Solter, M.D.Posthyperglycemic insulin area (uU/ml·min) 8,992.5 ± 756.2* 7,064.7 ± 425.9 ReferencesPosthyperglycemic insulin/ glucose area ratio 0.99 ± 0.13* 0.67 ± 0.05

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